Fundamental epidemiologic and pathophysiologic investigation of luteal phase defect will be undertaken in a two-part study. Epidemiologic studies of luteal phase defect will evaluate currently practiced clinical protocols for diagnosis of the disorder. Three timed late luteal phase endometrial biopsies in three separate cycles will be obtained from 100 presumably fertile and 200 infertile women. This will permit a description of the incidence of sporadic and persistent luteal phase defect among women in several subgroups defined according to reproductive status. The relationship between the results of two luteal phase evaluations using endometrial biopsy and the outcome of a third will be ascertained. A subset of the women studied will be observed without treatment, during subsequent efforts to conceive, which will permit a prospective assessment of the relevance of histologically determined luteal function to fecundity. Studies of pathophysiology and designed to clarify the relative role of progesterone availability and tissue sensitivity to progesterone in the genesis of luteal phase defect. The luteal phases of 20 women with luteal phase defect and 20 women with a normal luteal phase will be studied in detail. Daily (total & free) blood progesterone determinations and two 14-hour sequences of frequent (total & free) progesterone sampling will be used to attempt to correlate the occurrence of luteal phase defect with abnormalities in circulating available progesterone taking into account fluctuations in progesterone levels and plasma proteins binding of progesterone. Endometrial biopsies will be obtained on two occasions in these same luteal phases. This will provide data on the nature of development of the histologic deficit over time and biochemical studies in tissue culture will be used to ascertain endometrial responsiveness to progesterone in normal and abnormal luteal phases. These studies are designed to indicate whether luteal phase defect arises through progesterone inadequacy or inadequate tissue response to progesterone.